法國路易·巴斯德大學(xué)的研究人員最近開發(fā)出一種藥物,，能誘導(dǎo)脂肪燃燒來達到減肥目的,，使用這種藥物的實驗鼠即使大吃大喝也不會胖。
據(jù)英國《每日郵報》報道,，這種藥物還沒有正式名稱,，只是暫名為“SRT1720”，其作用與紅酒中所含的對人體有益的成分白藜蘆醇相似,，它們均能使一些哺乳動物體內(nèi)的“SIRT1”蛋白質(zhì)活躍起來,，而這種蛋白質(zhì)對調(diào)節(jié)體內(nèi)能量供應(yīng)起關(guān)鍵作用,。如果“SIRT1”蛋白質(zhì)比較活躍,，那么即使食物充足，它也能讓大腦認為需要燃燒儲備的脂肪來補充能量,，從而促進新陳代謝,。
目前，這種藥物已在實驗鼠身上進行了測試,，結(jié)果在“SRT1720”使用量較大的情況下,，實驗鼠連續(xù)10周食用高脂肪食物后體重也沒有增加，不過“SRT1720”使用量較小時效果不明顯,。
研究人員還發(fā)現(xiàn),，實驗鼠在大量攝入“SRT1720”后，其運動能力和耐心都有所增強,，同時沒有出現(xiàn)副作用,。這一研究已發(fā)表在11月5日美國《細胞—代謝》（Cell Metabolism）雜志上。
研究人員說,，希望能很快用“SRT1720”進行人體試驗,，并預(yù)計這種減肥藥有望在5年內(nèi)上市,。（生物谷Bioon.com）
生物谷推薦原始出處：
Cell Metabolism，Volume 8, Issue 5, 347-358, 5 November 2008,，Jér?me N. Feige, Peter J. Elliott and Johan Auwerx
Specific SIRT1 Activation Mimics Low Energy Levels and Protects against Diet-Induced Metabolic Disorders by Enhancing Fat Oxidation
Jérôme N. Feige1,Marie Lagouge1,Carles Canto1,Axelle Strehle1,Sander M. Houten2,Jill C. Milne3,Philip D. Lambert3,Chikage Mataki1,Peter J. Elliott3andJohan Auwerx1,4,5,
1 Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/Université Louis Pasteur, 67404, Illkirch, France
2 Academic Medical Center, University of Amsterdam, 1100DE Amsterdam, The Netherlands
3 Sirtris Pharmaceuticals Inc., 200 Technology Square, Cambridge, MA 02139, USA
4 Institut Clinique de la Souris, 67404, Illkirch, France
5 Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne (EPFL), CH-1015, Lausanne, Switzerland
The NAD+-dependent deacetylase SIRT1 controls metabolic processes in response to low nutrient availability. We report the metabolic phenotype of mice treated with SRT1720, a specific and potent synthetic activator of SIRT1 that is devoid of direct action on AMPK. SRT1720 administration robustly enhances endurance running performance and strongly protects from diet-induced obesity and insulin resistance by enhancing oxidative metabolism in skeletal muscle, liver, and brown adipose tissue. These metabolic effects of SRT1720 are mediated by the induction of a genetic network controlling fatty acid oxidation through a multifaceted mechanism that involves the direct deacetylation of PGC-1, FOXO1, and p53 and the indirect stimulation of AMPK signaling through a global metabolic adaptation mimicking low energy levels. Combined with our previous work on resveratrol, the current study further validates SIRT1 as a target for the treatment of metabolic disorders and characterizes the mechanisms underlying the therapeutic potential of SIRT1 activation.
